Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Kawasaki disease (KD) is a multisystemic vasculitis that often includes coronary artery involvement. The serum levels of matrix metalloproteinase (MMP)-3 and -9 are significantly elevated in KD patients, and polymorphisms in the genes encoding MMP-3 and MMP-9 have been associated with the susceptibility, severity, and progression of atherosclerosis and aneurysm. However, the association between MMP-3 gene polymorphisms and development of aneurysm is somewhat controversial in a number of diseases. Ninety-seven children with KD and 194 children with congenital heart disease (CHD) were included in this study. Echocardiography was used to examine all children in the KD group for coronary artery aneurysm. Genotyping of the MMP-3 (-439C/G) promoter polymorphism was performed using the single-base extension method, and serum MMP-3 levels were estimated using the sandwich enzyme immunoassay method. There was no significant difference in MMP-3 (-439C/G) genotypes between KD and control groups. There was no association between this MMP-3 polymorphism and development of coronary aneurysm in KD. Serum MMP-3 levels were significantly higher in KD patients compared to control subjects. Among the KD patients, serum MMP-3 levels were higher in children with genotypes CG+GG compared to the CC group, but this difference was not significant. Although further large-scale studies will be required to fully examine the relationship between MMP-3 gene polymorphisms and coronary artery lesions (CAL) in KD, the present findings suggest that while MMP-3 may play a role in the pathogenesis of KD, there is no apparent association between CAL and the MMP-3 (-439C/G) gene polymorphism in Korean children with KD.
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PMID:Association of the matrix metalloproteinase-3 (-439C/G) promoter polymorphism with Kawasaki disease in Korean children. 1881 May 83

When challenged by hemodynamic stress, aging hearts respond differently to young hearts. Preclinical models of heart disease should take into account the effects of age. However, in the transverse aortic constriction (TAC) model of pressure-overload cardiomyopathy, the larger aorta of aging mice has not previously been taken into account. First, we studied the aortic size in mice, and found that the aortic cross-sectional area (CSA) is 28% larger in aging mice than in young adult mice (P=0.001). We then performed TAC to make the same proportional reduction in CSA in young and aging mice. This produced the same pressure gradient across the constriction and the same rise in B-type natriuretic peptide expression. Young mice showed acute deterioration in systolic function assessed by pressure-volume loops, progressive LV remodeling on echocardiography, and a 50% mortality at 12 weeks post-TAC. In contrast, aging mice showed no acute deterioration in systolic function, much less ventricular remodeling and were protected from death. Aging mice also showed significantly increased levels of matrix metalloproteinase-3 (MMP-3; 3.2 fold increase, P<0.001) and MMP-12 (1.5-fold increase, P<0.001), which were not seen in young mice. Expression of tissue inhibitor of MMP-1 (TIMP-1) increased 8.6-fold in aging hearts vs 4.3-fold in young hearts (P<0.01). In conclusion, following size-appropriate TAC, aging mice exhibit less LV remodeling and lower mortality than young adult mice. This is associated with induction of protective ECM changes.
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PMID:Aging is protective against pressure overload cardiomyopathy via adaptive extracellular matrix remodeling. 2869 53